The Experts below are selected from a list of 273 Experts worldwide ranked by ideXlab platform
James W. Hodge - One of the best experts on this subject based on the ideXlab platform.
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The Use of Chelated Radionuclide (Samarium-153-Ethylenediaminetetramethylenephosphonate) to Modulate Phenotype of Tumor Cells and Enhance T Cell–Mediated Killing
Clinical Cancer Research, 2008Co-Authors: Mala Chakraborty, Jorge A Carrasquillo, Elizabeth K. Wansley, Kevin Camphausen, Jeffrey Schlom, Chang H. Paik, Michael Becker, William F Goeckeler, James W. HodgeAbstract:Purpose: Exposing human tumor cells to sublethal doses of external beam radiation up-regulates expression of tumor antigen and accessory molecules, rendering tumor cells more susceptible to killing by antigen-specific CTLs. This study explored the possibility that exposure to palliative doses of a Radiopharmaceutical Agent could alter the phenotype of tumor cells to render them more susceptible to T cell–mediated killing. Experimental Design: Here, 10 human tumor cell lines (4 prostate, 2 breast, and 4 lung) were exposed to increasing doses of the Radiopharmaceutical samarium-153-ethylenediaminetetramethylenephosphonate ( 153 Sm-EDTMP) used in cancer patients to treat pain due to bone metastasis. Fluorescence-activated cell sorting analysis and quantitative real-time PCR analysis for expression of five surface molecules and several tumor-associated antigens involved in prostate cancer were done. LNCaP human prostate cancer cells were exposed to 153 Sm-EDTMP and incubated with tumor-associated antigen-specific CTL in a CTL killing assay to determine whether exposure to 153 Sm-EDTMP rendered LNCaP cells more susceptible to T cell–mediated killing. Results: Tumor cells up-regulated the surface molecules Fas (100% of cell lines up-regulated Fas), carcinoembryonic antigen (90%), mucin-1 (60%), MHC class I (50%), and intercellular adhesion molecule-1 (40%) in response to 153 Sm-EDTMP. Quantitative real-time PCR analysis revealed additional up-regulated tumor antigens. Exposure to 153 Sm-EDTMP rendered LNCaP cells more susceptible to killing by CTLs specific for prostate-specific antigen, carcinoembryonic antigen, and mucin-1. Conclusions: Doses of 153 Sm-EDTMP equivalent to palliative doses delivered to bone alter the phenotype of tumor cells, suggesting that 153 Sm-EDTMP may work synergistically with immunotherapy to increase the susceptibility of tumor cells to CTL killing.
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the use of chelated radionuclide samarium 153 ethylenediaminetetramethylenephosphonate to modulate phenotype of tumor cells and enhance t cell mediated killing
Clinical Cancer Research, 2008Co-Authors: Mala Chakraborty, Jorge A Carrasquillo, Elizabeth K. Wansley, Kevin Camphausen, Jeffrey Schlom, Chang H. Paik, Michael Becker, William F Goeckeler, James W. HodgeAbstract:Purpose: Exposing human tumor cells to sublethal doses of external beam radiation up-regulates expression of tumor antigen and accessory molecules, rendering tumor cells more susceptible to killing by antigen-specific CTLs. This study explored the possibility that exposure to palliative doses of a Radiopharmaceutical Agent could alter the phenotype of tumor cells to render them more susceptible to T cell–mediated killing. Experimental Design: Here, 10 human tumor cell lines (4 prostate, 2 breast, and 4 lung) were exposed to increasing doses of the Radiopharmaceutical samarium-153-ethylenediaminetetramethylenephosphonate ( 153 Sm-EDTMP) used in cancer patients to treat pain due to bone metastasis. Fluorescence-activated cell sorting analysis and quantitative real-time PCR analysis for expression of five surface molecules and several tumor-associated antigens involved in prostate cancer were done. LNCaP human prostate cancer cells were exposed to 153 Sm-EDTMP and incubated with tumor-associated antigen-specific CTL in a CTL killing assay to determine whether exposure to 153 Sm-EDTMP rendered LNCaP cells more susceptible to T cell–mediated killing. Results: Tumor cells up-regulated the surface molecules Fas (100% of cell lines up-regulated Fas), carcinoembryonic antigen (90%), mucin-1 (60%), MHC class I (50%), and intercellular adhesion molecule-1 (40%) in response to 153 Sm-EDTMP. Quantitative real-time PCR analysis revealed additional up-regulated tumor antigens. Exposure to 153 Sm-EDTMP rendered LNCaP cells more susceptible to killing by CTLs specific for prostate-specific antigen, carcinoembryonic antigen, and mucin-1. Conclusions: Doses of 153 Sm-EDTMP equivalent to palliative doses delivered to bone alter the phenotype of tumor cells, suggesting that 153 Sm-EDTMP may work synergistically with immunotherapy to increase the susceptibility of tumor cells to CTL killing.
Mala Chakraborty - One of the best experts on this subject based on the ideXlab platform.
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The Use of Chelated Radionuclide (Samarium-153-Ethylenediaminetetramethylenephosphonate) to Modulate Phenotype of Tumor Cells and Enhance T Cell–Mediated Killing
Clinical Cancer Research, 2008Co-Authors: Mala Chakraborty, Jorge A Carrasquillo, Elizabeth K. Wansley, Kevin Camphausen, Jeffrey Schlom, Chang H. Paik, Michael Becker, William F Goeckeler, James W. HodgeAbstract:Purpose: Exposing human tumor cells to sublethal doses of external beam radiation up-regulates expression of tumor antigen and accessory molecules, rendering tumor cells more susceptible to killing by antigen-specific CTLs. This study explored the possibility that exposure to palliative doses of a Radiopharmaceutical Agent could alter the phenotype of tumor cells to render them more susceptible to T cell–mediated killing. Experimental Design: Here, 10 human tumor cell lines (4 prostate, 2 breast, and 4 lung) were exposed to increasing doses of the Radiopharmaceutical samarium-153-ethylenediaminetetramethylenephosphonate ( 153 Sm-EDTMP) used in cancer patients to treat pain due to bone metastasis. Fluorescence-activated cell sorting analysis and quantitative real-time PCR analysis for expression of five surface molecules and several tumor-associated antigens involved in prostate cancer were done. LNCaP human prostate cancer cells were exposed to 153 Sm-EDTMP and incubated with tumor-associated antigen-specific CTL in a CTL killing assay to determine whether exposure to 153 Sm-EDTMP rendered LNCaP cells more susceptible to T cell–mediated killing. Results: Tumor cells up-regulated the surface molecules Fas (100% of cell lines up-regulated Fas), carcinoembryonic antigen (90%), mucin-1 (60%), MHC class I (50%), and intercellular adhesion molecule-1 (40%) in response to 153 Sm-EDTMP. Quantitative real-time PCR analysis revealed additional up-regulated tumor antigens. Exposure to 153 Sm-EDTMP rendered LNCaP cells more susceptible to killing by CTLs specific for prostate-specific antigen, carcinoembryonic antigen, and mucin-1. Conclusions: Doses of 153 Sm-EDTMP equivalent to palliative doses delivered to bone alter the phenotype of tumor cells, suggesting that 153 Sm-EDTMP may work synergistically with immunotherapy to increase the susceptibility of tumor cells to CTL killing.
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the use of chelated radionuclide samarium 153 ethylenediaminetetramethylenephosphonate to modulate phenotype of tumor cells and enhance t cell mediated killing
Clinical Cancer Research, 2008Co-Authors: Mala Chakraborty, Jorge A Carrasquillo, Elizabeth K. Wansley, Kevin Camphausen, Jeffrey Schlom, Chang H. Paik, Michael Becker, William F Goeckeler, James W. HodgeAbstract:Purpose: Exposing human tumor cells to sublethal doses of external beam radiation up-regulates expression of tumor antigen and accessory molecules, rendering tumor cells more susceptible to killing by antigen-specific CTLs. This study explored the possibility that exposure to palliative doses of a Radiopharmaceutical Agent could alter the phenotype of tumor cells to render them more susceptible to T cell–mediated killing. Experimental Design: Here, 10 human tumor cell lines (4 prostate, 2 breast, and 4 lung) were exposed to increasing doses of the Radiopharmaceutical samarium-153-ethylenediaminetetramethylenephosphonate ( 153 Sm-EDTMP) used in cancer patients to treat pain due to bone metastasis. Fluorescence-activated cell sorting analysis and quantitative real-time PCR analysis for expression of five surface molecules and several tumor-associated antigens involved in prostate cancer were done. LNCaP human prostate cancer cells were exposed to 153 Sm-EDTMP and incubated with tumor-associated antigen-specific CTL in a CTL killing assay to determine whether exposure to 153 Sm-EDTMP rendered LNCaP cells more susceptible to T cell–mediated killing. Results: Tumor cells up-regulated the surface molecules Fas (100% of cell lines up-regulated Fas), carcinoembryonic antigen (90%), mucin-1 (60%), MHC class I (50%), and intercellular adhesion molecule-1 (40%) in response to 153 Sm-EDTMP. Quantitative real-time PCR analysis revealed additional up-regulated tumor antigens. Exposure to 153 Sm-EDTMP rendered LNCaP cells more susceptible to killing by CTLs specific for prostate-specific antigen, carcinoembryonic antigen, and mucin-1. Conclusions: Doses of 153 Sm-EDTMP equivalent to palliative doses delivered to bone alter the phenotype of tumor cells, suggesting that 153 Sm-EDTMP may work synergistically with immunotherapy to increase the susceptibility of tumor cells to CTL killing.
Dmitri V Krysko - One of the best experts on this subject based on the ideXlab platform.
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noninvasive whole body imaging of phosphatidylethanolamine as a cell death marker using 99mtc duramycin during tnf induced sirs
The Journal of Nuclear Medicine, 2018Co-Authors: Tinneke Delvaeye, Leonie Wyffels, Steven Deleye, Kelly Lemeire, Amanda Goncalves, Elke Decrock, Steven Staelens, Luc Leybaert, Peter Vandenabeele, Dmitri V KryskoAbstract:Systemic inflammatory response syndrome (SIRS) is an inflammatory state affecting the whole body. It is associated with the presence of pro- and anti-inflammatory cytokines in serum, including tumor necrosis factor (TNF). TNF has multiple effects and leads to cytokine production, leukocyte infiltration, blood pressure reduction and coagulation, thereby contributing to tissue damage and organ failure. A sterile mouse model of sepsis, TNF-induced SIRS, was used to visualize the temporal and spatial distribution of damage in susceptible tissues during SIRS. For this, a Radiopharmaceutical Agent, 99mTc-duramycin, binding to exposed phosphatidylethanolamine on dying cells, was longitudinally visualized using single photon emission computed tomography (SPECT/CT) imaging. Methods: C57Bl/6J mice were challenged with intravenous (i.v.) injections of murine TNF or vehicle, and necrostatin-1 (Nec-1) was used to interfere with cell death. Two h post vehicle- or TNF-treatment, mice received 99mTc-duramycin i.v. (35.44±3.80 MBq). Static whole-body 99mTc-duramycin SPECT/CT imaging was performed 2, 4 and 6 h post-tracer injection. Tracer uptake in different organs was quantified by volumes of interest analysis using PMOD software and expressed as mean Standard Uptake Value (SUVmean). After the last scan, ex vivo biodistribution was performed to validate the SPECT imaging data. Lastly, terminal deoxynucleotidyl-transferase mediated deoxyuridine triphosphate nick-end labeling (TUNEL) staining was performed to correlate the obtained results to cell death. Results: An increased 99mTc-duramycin uptake was detected in mice injected with TNF, when compared to control mice in lungs (0.55±0.05 vs 0.34±0.03), intestine (0.75±0.06 vs 0.56±0.05) and liver (1.03±0.09 vs 0.64±0.02) 4 h post TNF, and remained significantly elevated until 8 h post TNF. The imaging results were consistent with ex vivo γ-counting results. Significant increased levels of tissue damage were detected via TUNEL staining in the lungs and intestine of mice injected with TNF. Interestingly, Nec-1 pretreatment conferred protection against lethal SIRS and reduced the 99mTc-duramycin-uptake in the lungs, 8 h post TNF (SUV = 0.32±0.04 vs 0.51±0.08). Conclusion: This study demonstrates that noninvasive 99mTc-duramycin SPECT imaging can be used to characterize temporal and spatial kinetics of injury and cell death in susceptible tissues during TNF-induced SIRS, making it useful for global, whole-body assessment of tissue damage during diseases associated with inflammation and injury.
Minzan Zuo - One of the best experts on this subject based on the ideXlab platform.
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Progress in the mechanism and drug development of castration-resistant prostate cancer
Future medicinal chemistry, 2016Co-Authors: Minzan ZuoAbstract:Although prostate cancer can initially respond to androgen deprivation therapy, it will inevitably relapse and switch to a castration-resistant state. The progress in understanding the mechanism of castration-resistant prostate cancer (CRPC) has led to the evolution of novel Agents, including sipuleucel-T as an immunomodulant Agent, enzalutamide as an androgen receptor antagonist, docetaxel as a chemotherapeutic Agent and radium-223 as a Radiopharmaceutical Agent. In this review, we discuss the main mechanisms of CRPC and the development of promising Agents along with the novel therapies in the clinic. New therapeutic challenges remain, such as the identification of predictive biomarkers and the optimal combinations of Agents. Future investigation is still needed for a better understanding of CRPC.
Kevin Camphausen - One of the best experts on this subject based on the ideXlab platform.
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The Use of Chelated Radionuclide (Samarium-153-Ethylenediaminetetramethylenephosphonate) to Modulate Phenotype of Tumor Cells and Enhance T Cell–Mediated Killing
Clinical Cancer Research, 2008Co-Authors: Mala Chakraborty, Jorge A Carrasquillo, Elizabeth K. Wansley, Kevin Camphausen, Jeffrey Schlom, Chang H. Paik, Michael Becker, William F Goeckeler, James W. HodgeAbstract:Purpose: Exposing human tumor cells to sublethal doses of external beam radiation up-regulates expression of tumor antigen and accessory molecules, rendering tumor cells more susceptible to killing by antigen-specific CTLs. This study explored the possibility that exposure to palliative doses of a Radiopharmaceutical Agent could alter the phenotype of tumor cells to render them more susceptible to T cell–mediated killing. Experimental Design: Here, 10 human tumor cell lines (4 prostate, 2 breast, and 4 lung) were exposed to increasing doses of the Radiopharmaceutical samarium-153-ethylenediaminetetramethylenephosphonate ( 153 Sm-EDTMP) used in cancer patients to treat pain due to bone metastasis. Fluorescence-activated cell sorting analysis and quantitative real-time PCR analysis for expression of five surface molecules and several tumor-associated antigens involved in prostate cancer were done. LNCaP human prostate cancer cells were exposed to 153 Sm-EDTMP and incubated with tumor-associated antigen-specific CTL in a CTL killing assay to determine whether exposure to 153 Sm-EDTMP rendered LNCaP cells more susceptible to T cell–mediated killing. Results: Tumor cells up-regulated the surface molecules Fas (100% of cell lines up-regulated Fas), carcinoembryonic antigen (90%), mucin-1 (60%), MHC class I (50%), and intercellular adhesion molecule-1 (40%) in response to 153 Sm-EDTMP. Quantitative real-time PCR analysis revealed additional up-regulated tumor antigens. Exposure to 153 Sm-EDTMP rendered LNCaP cells more susceptible to killing by CTLs specific for prostate-specific antigen, carcinoembryonic antigen, and mucin-1. Conclusions: Doses of 153 Sm-EDTMP equivalent to palliative doses delivered to bone alter the phenotype of tumor cells, suggesting that 153 Sm-EDTMP may work synergistically with immunotherapy to increase the susceptibility of tumor cells to CTL killing.
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the use of chelated radionuclide samarium 153 ethylenediaminetetramethylenephosphonate to modulate phenotype of tumor cells and enhance t cell mediated killing
Clinical Cancer Research, 2008Co-Authors: Mala Chakraborty, Jorge A Carrasquillo, Elizabeth K. Wansley, Kevin Camphausen, Jeffrey Schlom, Chang H. Paik, Michael Becker, William F Goeckeler, James W. HodgeAbstract:Purpose: Exposing human tumor cells to sublethal doses of external beam radiation up-regulates expression of tumor antigen and accessory molecules, rendering tumor cells more susceptible to killing by antigen-specific CTLs. This study explored the possibility that exposure to palliative doses of a Radiopharmaceutical Agent could alter the phenotype of tumor cells to render them more susceptible to T cell–mediated killing. Experimental Design: Here, 10 human tumor cell lines (4 prostate, 2 breast, and 4 lung) were exposed to increasing doses of the Radiopharmaceutical samarium-153-ethylenediaminetetramethylenephosphonate ( 153 Sm-EDTMP) used in cancer patients to treat pain due to bone metastasis. Fluorescence-activated cell sorting analysis and quantitative real-time PCR analysis for expression of five surface molecules and several tumor-associated antigens involved in prostate cancer were done. LNCaP human prostate cancer cells were exposed to 153 Sm-EDTMP and incubated with tumor-associated antigen-specific CTL in a CTL killing assay to determine whether exposure to 153 Sm-EDTMP rendered LNCaP cells more susceptible to T cell–mediated killing. Results: Tumor cells up-regulated the surface molecules Fas (100% of cell lines up-regulated Fas), carcinoembryonic antigen (90%), mucin-1 (60%), MHC class I (50%), and intercellular adhesion molecule-1 (40%) in response to 153 Sm-EDTMP. Quantitative real-time PCR analysis revealed additional up-regulated tumor antigens. Exposure to 153 Sm-EDTMP rendered LNCaP cells more susceptible to killing by CTLs specific for prostate-specific antigen, carcinoembryonic antigen, and mucin-1. Conclusions: Doses of 153 Sm-EDTMP equivalent to palliative doses delivered to bone alter the phenotype of tumor cells, suggesting that 153 Sm-EDTMP may work synergistically with immunotherapy to increase the susceptibility of tumor cells to CTL killing.
